Evidence map›Paper›PMID 33936025›Full record

ArticleFrontiers in immunology2021

Elevated microRNA-21 Is a Brake of Inflammation Involved in the Development of Nasal Polyps.

Ruowu Liu, Jintao Du, Jiao Zhou, Bing Zhong, Luo Ba, Jie Zhang, Yafeng Liu, Shixi Liu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 31 citations in OpenAlex.

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  3. Potential roles of microRNAs in chronic rhinosinusitis: from mechanistic insights to clinical studies.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Ruowu LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Jintao DuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Jiao ZhouState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Bing ZhongDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Luo BaDepartment of Otolaryngology, People's Hospital of the Tibet Autonomous Region, Lasha, China.
Jie ZhangState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yafeng LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Shixi LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
West China Hospital of Sichuan University · CNSichuan University · CNState Key Laboratory of BiotherapyTibet Autonomous Region People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: CRSwNP is an inflammatory disease but the mechanism is not yet fully understood. MiR-21, a member of miRNAs, has been reported to play roles in mediating inflammation. However, the expression of miR-21 and its role in patients with CRSwNP remain elusive. Methods: Turbinates from control subjects, uncinate processes from CRSsNP, polyp tissues from CRSwNP, and nasal epithelial cells brushed from nasal mucosa were collected. The expression of miR-21 and cytokines in nasal tissues and epithelial cells were detected by qPCR. The localization of miR-21 was detected by ISH, and its target was identified by bioinformation analysis, qPCR, IHC, WB, and luciferase reporter system. The protein and mRNA of PDCD4 and NF-κB P65 were determined by WB and qPCR after miR-21 transfection in HNEpC. The role of miR-21 on cytokines was analyzed in HNEpC and nasal polyp explants. Results: MiR-21 was upregulated in CRSwNP relative to control subjects by qPCR, which was determined mainly in nasal epithelial cells of CRSwNP by ISH. Both pro-inflammation cytokines (IL-1β, IL-6, IL-8, IL-25, and TSLP) and a suppressive cytokine (IL-10) were overexpressed in the epithelial cells of CRSwNP. The expression of miR-21 was positively correlated with IL-10 and negatively correlated with IL-6, IL-8, IL-33, and TSLP in the epithelial cells of CRSwNP. As a potential target of miR-21, the expression of PDCD4 was negatively correlated with miR-21 in CRSwNP. In HNEpC, miR-21 could reduce the expression of PDCD4 at both mRNA and protein levels, and bioinformation analysis and luciferase reporter system confirmed PDCD4 as one target of miR-21. Furthermore, miR-21 could decrease the activation of NF-κB and increase IL-10 mRNA. Both SEB and LPS could elevate miR-21, with IL-25, IL-33, TSLP induced by SEB and IL-1β, IL-6, IL-8 induced by LPS, while the miR-21 could regulate the expression of IL-33, TSLP, IL-1β, IL- 6 and IL-8 Conclusion: MiR-21 could be a prominent negative feedback factor in the inflammation process to attenuate the expression of pro-inflammatory cytokines, thereby playing an anti-inflammation role in CRSwNP.

Indexed as

AdolescentAdultApoptosis Regulatory ProteinsCell LineChronic DiseaseCytokinesEpithelial CellsFemaleGene Expression RegulationHumansInflammationLipopolysaccharidesMaleMicroRNAsMiddle AgedNasal MucosaApoptosis Regulatory ProteinsCytokinesLipopolysaccharidesMicroRNAsMIRN21 microRNA, humanPDCD4 protein, humanRNA-Binding ProteinsTranscription Factor RelAchronic rhinosinusitiscytokinesmiR-21nasal epithelial cellsnasal polypsPDCD4

Identifiers

PMID33936025
PMCPMC8082185
OpenAlexW3156033787

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.